PDGFRA (Platelet Derived Growth Factor Receptor Alpha)

Molecular docking analyses suggested potential interactions with several signaling proteins, including Src, MAPK14, GSK3β, PDGFRA, and VEGFR2. Collectively, these findings identify compounds 26 and 27 as biologically active purine analogues with promising anti-HGSOC activity and support further evaluation in advanced preclinical models.

P3, N=450, GlaxoSmithKline

Despite histologic similarity, anogenital BCC demonstrates a distinct molecular profile, suggesting an alternative pathogenesis. Further genomic studies are warranted.

Targeted inhibition of TNT-mediated mitochondrial transfer markedly suppresses TB in TBO and xenograft models. Together, our results reveal a mechano-metabolic symbiosis between PDGFRα+/integrin α2+ CAFs and OSCC cells that drives TB and provides actionable targets to block this aggressive metastatic precursor.

Addressing these challenges requires​ thorough correlation with clinical and radiological findings, combined application of both immunohistochemical markers, and proactive genetic testing for cases with atypical immunohistochemical profile. These measures are crucial for improving diagnostic accuracy and guiding targeted therapies.

At follow-up, the patient was clinically stable and enrolled in a multidisciplinary surveillance program. This case highlights the importance of recognizing atypical hematologic presentations of GIST and the need for comprehensive molecular and genetic evaluation in young patients.

Both in vitro and in vivo experiments have validated the therapeutic efficacy and molecular mechanisms of IL-11-neutralizing antibodies in pulmonary fibrosis, offering promising insights for future anti-fibrotic drug development. Abbreviations: IL-11, Interleukin-11; IPF, Idiopathic pulmonary fibrosis; TGF-β, Transforming growth factor-β; NOX4, NADPH oxidase-4; SASP, Senescence-associated secretory phenotype; ECM, Extracellular matrix; α-SMA, α-smooth muscle actin; STAT3, Signal transducer and activator of transcription 3; ERK, Extracellular regulated protein kinases; AKT, Protein kinase B; BLM, Bleomycin; WT, Wild-type; KO, Knockout; qRT-PCR, Quantitative real-time polymerase chain reaction; WB, Western blot; hAb, Humanized antibody; mAb, Monoclonal antibody; FVC, Forced vital capacity; CTGF, Connective tissue growth factor; PDGFR-α, Platelet-derived growth factor receptor-α; TNF-α, Tumor necrosis factor-α; Nrf2, NFE2-related factor 2; EMT, Epithelial-mesenchymal transition; HE, Hematoxylin and eosin; PVDF, Polyvinylidene fluoride; GAPDH, Glyceraldehyde-3-phosphate dehydrogenase; siRNA, Small interfering RNA; IL-6, Interleukin-6; MEK, Mitogen-Activated Protein Kinase Kinase; TIME, TGF-β1/IL-11/MEK/ERK; HRP, Horseradish Peroxidase; MLG, Mouse lung fibroblast cell line MLg; NCBI, National Center for Biotechnology Information; Bcl2, BCL2 apoptosis regulator; Bax, BCL2 Associated X, apoptosis regulator; MSC, Mesenchymal Stem Cell; RSK, p90 Ribosomal S6 Kinase; KD, Dissociation Constant; Nin, Nintedanib; CTL, Control; Eto, Etoposide; SA-β-Gal, Senescence-Associated β-Galactosidase.

Anti-PDGFRα autoantibody is a novel biomarker for early diagnosis and poor prognosis of NSCLC. The mechanisms exploration may provide the theoretical basis for the precision treatment of NSCLC targeting anti-PDGFRα autoantibody.

We describe a case of complete and durable remission achieved with imatinib monotherapy in an unresectable mesenteric desmoid tumour with the patient remaining disease-free at 10 years. This case highlights the potential for long-term complete response and underscores the need for prospective data to guide treatment duration and cessation criteria.

Despite these advances, OPC differentiation and maturation efficiencies remained suboptimal, highlighting the need for further optimization. Collectively, our findings establish a scalable and time-efficient strategy for iPSC-derived OPC generation and underscore their potential for disease modeling and cell-based remyelination therapies.

The reported case underscores the diagnostic complexity and difficulties in managing hypereosinophilia of undetermined significance in clinical practice. While current evidence suggests a generally benign course, rare progression to hypereosinophilic syndrome or other malignancies requires structured long-term monitoring and individualized therapeutic decision-making.

Genome-wide SNP-based LOH profiling reveals distinct, subgroup-specific patterns of chromosomal imbalance in GIST and may serve as a feasible complementary approach to driver mutation analysis for refined molecular characterization and potential future clinical utility.